Obstructive Jaundice

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Obstructive Jaundice Whipples Operation
Anesthetic Management

• Munisha Agarwal
• Professor
• Deptt. of Anaesthesiology
• Intensive Care
• L N Hospital Maulana
• Azad Medical College Delhi

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
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Obstructive Jaundice

• Physiological functions of Liver ?

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Physiological functions of Liver

• Glucose Homeostasis
• Fat Metabolism
• Protein Synthesis
• Drug Hormone Metabolism
• Bilirubin formation excretion
• Anti bacterial action
• Blood Reservoir

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Glucose homeostasis

• Glucose hepatocytes glycogen glucose
• lactate
• glycerol
• AA

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Glucose Homeostasis

• Glycogen stores 75gm 2448hrs
• Anesthesia gluconeogenesis
• Provide ext. source of glucose

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Fat metabolism

• Synthesis of lipo-proteins cholesterol
• Oxidation of FA to ketone bodies

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Protein Metabolism

• Deamination of AA
• Formation of urea
• Plasma proteins
• - All except y globulin factor VIII
• - Albumin daily prod. 1015g/d (3.5-5.5gm)
• - liver disease ? alb ? glob
• Albumin ?

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Protein synthesis

• Plasma O. P.
• Drug binding
• Coagulation
• Hydrolysis

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Drug binding

• Drugs reversibly combine with Albumin
• ? albumin ? binding sites ? free drug
• Albumin lt 2.5gm
• Acute Hepatic dysfunction ?
• Coagulation ?

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Drug binding

• Acute hepatic dysfunction - drug binding not
  affected
• T ½ Albumin 14 21 days
• Coagulation affected (26hrs)
• Vitamin K dependent Coag. Factors?

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Coagulation

• Prothrombin, fibrinogen
• Factor V, VII, IX, X ( except VIII)
• Deranged Coagulation ?

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Coagulation

• Deranged coagulation
• ?ed synthesis of Clotting factors
• ?ed PT Vit. K deficiency d/t biliary
  obstruction ?absence of bile salts
• Thrombocytopenia
• ?ed Fibrinolysins

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Coagulation

• Evaluate PT/ PTTK/ BT
• LFT grossly deranged before coagulation
  abnormalities appear
• 20--30 activity required for normal coagulation
• T1/2 of clotting factors produced in liver is
  very short (in hrs)
• Ac. Hep dysfunction ? Coag. Abn.

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Drug metabolism

• - Lipophilic ?water soluble, less reactive
• Enzymatic reaction
• phase I - oxidation (Cyt P450)
• - reduction hydrolysis
  (L.A)
• phase II - conjugation, glucuronidation,
• sulphation, methylation
• acetylation
• - UDGT ( Bilirubin,
  morphine,
  
• aminophylline)
• Conjugation reaction?

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Drug metabolism

• Clearance of drugs from plasma
• High HE ratio Hepatic Blood Flow (HBF)
  Lidocain, Pethidine, Fentanyl
• low HE ratio microsomal enzymes
• protein binding
• diazepam, thiop, pancuronium

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Drug metabolism

• Anesthetic implications
• Chronic liver disease ?? drug metabolism d/t
  - ?ed no. of hepatocytes
• - HBF
• Repeated injection ? cumulative effect
• Volatile anesth. Agents ? ?ed clearance of drugs

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Bilirubin formation excretion

• Daily prod 250350mg/d
• Interpretation of plasma urine bilirubin
• Categories of liver dysfunction
• 1 unit BT ?

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Blood Reservoir

• 10 of total blood volume
• Available for Auto transfusion into central
  circulation

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Hepatic Blood Supply

• Unique ?

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Hepatic Blood Supply

• 25 to 30 of CO
• Dual supply
• Portal V (75) 85 saturated
• Hepatic A (25) 95saturated
• 2/3 of oxygen used by liver

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Control of Liver Blood Flow

• INTRINSIC
• AUTOREGULATION
• - Hepatic artery-80 mmHg
• - Portal vein flow from spleen, intestine
• - resistance to vascular
  bed
• Hepatic Arterial Buffer response.
• Extrinsic ?

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Control of Liver Blood Flow
EXTRINSIC

• Decrease HBF
• Hypoxia
• Hepatic cirrhosis
• Upright posture
• Hypocapnia/IPPV/PEEP
• Drugs
• ßadrenoreceptor blockade/ a agonist
• Ganglion blockade
• Anaesthetic agent

• Increase HBF
• Acute hepatitis
• Supine posture
• Hypercapnia
• Drugs
• ßadrenostimulation

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Liver Function Tests

• Non specific
• Large hepatic reserve
• LFT ?

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Liver Function Tests

• S. Bilirubin (T) - 0.31.1mg
• (I) 0.2-0.7mg, (D)0.10.4mg)
• TransaminasesSGOT/SGPT/LDH
• hepatocyte damage hypoxia/drugs/viruses
• Extrahepaticheart/lungs/skeletal ms
• Marked? (3x)-ac. Hep damage
• Alkaline phoshphatase - bile duct cells
• slight obstruction (3x)
• bone extrahep source
• S. Albumin
• 5- Nucleotidase
• GGT
• Prehepatic / Hepatic / Posthepatic J ?

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Hepatic dysfunction Bilirubin Transaminase enzyme Alkalinephosph. Causes
Pre hepatic Unconjug ated (indirect) Normal Normal Hemolysis/ hematoma resorp./ bilirubin overload-BT
Intrahepatic(hepatocellular) Conjugated(direct) elevated Normal to Slightly ? Viral/drugs/sepsis/hypoxia/cirrhosis
Posthepatic (cholestatic) conjugated Nomal to slightly ?ed ? (2x) Stones, Sepsis, tumor
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SPECTRUM OF LIVER DISEASE

• Parenchymal-Acute Chronic Hepatitis
• -Hepatic Cirrhosis ( portal
• 
  hypertension)
• Cholestatic -Intrahepatic viral hepatitis
• drug induced
• -Extrahepatic (Obstructive
  jaundice)
• Calculi, stricture, growth.
• Parenchymal disease ultimately possesses an
  obstructive component Obstructive disease
  produces cellular dysfunction.
• Clinical Hallmarks ?

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Signs Symptoms

• Prog sev jaundice
• Dark urine
• Clay coloured stools
• Pruritis
• High fever chills
• Biochemical hallmarks

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Obstructive Jaundice

• Primary mechanism- Obst. of E.H. bile duct.
• Bile duct pressure -
• Normal 10-15 cm H2O
• gt 15 cm ? bile flow decreases
• gt 30 cm ? bile flow stops

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Pathophysiological consequences
Bile Acids are potent toxins
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Endotoxemia in obstructive jaundice

• Bile salts are surfactants----disrupt endotoxins
• Causes of endotoxemia
• Absence of bile in intestine ? ?intest.bact.
  Flora
• Breakdown of GI mucos. barrier- ?bact.
  translocation
• ?Hepatic RES function ? ?clearance of endotoxins
• Systemic Alterations CVS ?

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Systemic alterations

• Circulatory homeostasis
• CHOLEMIA ? ? vasodepressor effect on BVs
• ? cardiodepressor ? LVF
• ? ? PVR ? ? BP ? sympath
  renal cerebral vasoconstriction
• ? redistribution of TBV ?
  trapping of blood in splanc. Circulation ?
  ? effective BV
• ? NO - insensitive to
  vasoconstrictors
• ? Hypotension circulatory collapse

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Renal system

• Mild renal vasoconstriction
• Renal hypoperfusion( hypovolemia)
• Refractoriness of tubules to ADH
• Endotoxemia

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Renal System

• Acute Renal Failure

• Hepatorenal Syndrome

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Renal system
Hepatorenal Syndrome

• Oliguria
• Inability to excrete Na in urine( 10mmol/l)
• Functional change
• Normal renal blood flow
• Treatment Prevention-identify high risk
  patients

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Systemic alterations

• Coagulopathy(low grade DIC)
• Impaired platelet function
• ? FDP---inhibition of fibrinolysis
• ? Endotoxins
• Hm gastritis stress ulcers
• Impaired wound healing

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• Anesthetic problems in Obstructive Jaundice ?

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PROBLEMS

• DUE TO DYSFUNCTION OF LIVER ITSELF
• - Low serum proteins
• - Coagulopathy
• - Drug metabolism and disposition
• - Metabolic derangement - Hypoglycemia
• - Electrolyte
  imbalance
• - Haematological - Anaemia
• Thrombocytopenia
• Leucopenia
• DIC
• - Deficiency of fat soluble vitamins (A, D, E, K)
• - Increased serum cholesterol (atheromatous
  changes)

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PROBLEMS

• DUE TO INVOLVEMENT OF OTHER SYSTEMS
• CVS TBV ?, PVR ?, ?Circulatory collapse
• Renal - pre renal azotemia
• - Hepatorenal failure
• GIT - Hm gastritis stress ulcers
• Resp. Arterial Hypoxemia
• - vulnerability to pulmonary infection
• CNS Hepatic encephalopathy
• Problems related to surgery ?

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Problems related to surgery

• Whipples procedure---Carc. Head of panc
• Distal gastrectomy,PJ, HJ, GJ
• Major surgery---long duration
• Increased blood loss/fluid shifts
• Wide incision---Roof topwarrants good
  postoperative analgesia
• Extensive monitoring reqd for favourable outcome

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Risk Factors

• Age gt 60yrs
• Albumin lt 30gm
• Preop. renal dysfunction
• Long standing biliary obstruction ? infection ?
  sepsis
• Weight loss
• ?Serum creatinine Sepsisprognostic factors
• ?Periop CVS collapse renal failure

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Preoperative Assessment

• OBJECTIVES
• Assess the type and degree of liver dysfunction.
• Assess effect on other system.
• To ensure post operative facilities (High risk
  patient).

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Preoperative Assessment

• History
• Clinical examination
• Investigations ???
• Unexplained jaundice of 4wks duration or longer
• will prove to be caused by obstruction in nearly
• 75 patients
• 
  Blumgart L

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Preoperative Investigations

• To know the pattern of disease
• S. Bilirubin
• SGOT, SGPT 90 predictive
• alk. phosphatase

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Preoperative Investigations

• To judge the synthetic ability of liver
• Serum albumin lt 25 gm - severe damage
• Albumin/globulin ratio reversed.
• Prothrombin time gt 15 sec. Over control
• INR - gt 1.3
• (D/D Par entral Vit. K Obst. Jaundice)

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To assess general condition of patient

• (i) Haematological Hb
• TLC, DLC
• Platelet Count Clotting factors (PT, PTTK)
  
• BT
• (ii)Cardiorespiratory
• Chest X-ray
• ECG
• Blood gases

• (iii) Metabolic-
• Serum proteins
• Serum glucose
• Electrolyte
• Urea / Creatinine
• Urinary-Urea/ Creatinine
• -Electrolyte
• (iv) Hepatic imaging
• (v) Microbiological
• - Culture
• - Hep. B marker
• - Viral antibodies

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Preoperative management

• Avoid prolonged hyperbilirubinemia
• Treat infection cholangitis
• Use Aminoglycosides carefully
• Avoid pre renal failure
• Correct Anaemia/Coagulation/hypoalbuminemia
• Avoid all NSAIDS
• I/V saline mannitol pre postop

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Preoperative management

• No conclusive evidence for
• Preop percutaneous biliary drainage
• Gut sterlization
• Polymyxin B
• Oral bile salts
• Pre medication ?

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Premedication

• Anxiolytic oral short acting BDZ
• Oral H2 antagonist
• Vit. K (Obst. J) 10 mg B D X 3 day
• If Bilirubin gt 8 mg
• I/V fluid 1-2 ml/kg/hr.
• Mannitol 100 ml of 20 2 hrs preop.
• Order morning PT / S. Electrolyte
• Preop urinary catheter CVP

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Anaesthetic Management

• General Considerations
• Minimize physiological insult to liver kidney
• Maintain O2 supply demand relationship in
  liver.
• ?Adequate pulmonary ventilation and
  cardiovascular fn.
• Maintain renal perfusion
• ?Avoid Hypotension, hypoproteinemia Hypoxia
  
• ? meticulous fluid balance
• Choose appropriate anaesthetic agent
• Metabolism of drugs Effect on HBF.
• Induction ?

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Anesthetic technique

• General anesthesia
• Preoxygenation
• Induction - Thiopentone
• Propofol
• Muscle relaxant
• Suxamethonium
• Vecuronium 0.15mg/kg
  Rocuronium0.6mg/kg
• Atracurium(DOC)
• Opioids ?

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Anesthetic technique

• Opioids Well tolerated
• smaller doses
• Morphineph-II reac.
• fentanyl(DOC)
• spasm of sphincter of Oddi

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Anesthetic technique

• Spasm of sphincter of Oddi
• Interpretation of operative cholangiography
  biliary pressures
• All patients do not show this response
• Incidence of spasm is very low
• Intraop manipulation of BD system ? spasm
• Treatment

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Anesthetic technique

• Volatile Anesthetics
• Useful well tolerated
• Can be entirely eliminated
• Disadv- CVS instability ? vasodilation ? ?perf.
  Press. ? ? blood velocity ?? oxygen extraction ?
  ? HBF oxygen supply
• Isofluranebest maint. of HBF oxygen
• IPPV ?

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Anesthetic technique

• IPPV
• - Maintain eucapnia
• - Liver low pr.tissue bed
• - Avoid large VT high airway pressures

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Anesthetic technique

• Maintenance of BV and Renal function
• Mannitol
• Frusemide
• Dopamine
• Adequate blood/component replacement

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Monitoring

• BP,HR,SpO2
• EtCO2
• CVP
• Urine output
• Core temp
• NMJ monitoring
• Blood loss

Biochemical B.Sugar,ABG S.Electrolytes Hematologi
cal Hb,PT,,PTTK,TEG
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Postoperative management

• All well ? Extubate
• Unstable
• - Continue IPPV in Post.op. period
• - Fluid Electrolyte imbalance
• corrected
• - CVS stability achieved.
• - Hypothermia corrected.
• - Urine Output 1 ml/kg/hr.
• Adequate analgesia (Small doses)
• Blood / blood product replaced.
• Antibiotics H2 receptor antagonist

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Thank You
www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om